Coconut Oil and the Boost in HDL “Good” Cholesterol

The effects of coconut oil were compared to butter and tallow. Even if virgin coconut oil and other saturated fats raise LDL “bad” cholesterol, isn’t that countered by the increase in HDL “good” cholesterol?

According to “the experience and wisdom of 200 of the country’s leading experts in cardiovascular diseases,” in a report representing 29 national medical organizations, including the American Heart Association and the American College of Cardiology, we’ve known for nearly half a century that “coconut oil is one of the most potent agents for elevating [blood] serum cholesterol level.” As I discuss in my video Coconut Oil and the Boost in HDL “Good” Cholesterol, studies showing coconut oil elevates cholesterol date back to 1955, when it was first shown experimentally that switching someone from coconut oil to soybean oil could drop cholesterol from around 200 down to 150, as you can see at 0:39 in my video.

Coconut oil can significantly raise cholesterol levels within hours of consumption. In fact, a significant increase in blood cholesterol was found within hours of eating a slice of cake made from either coconut oil (or cod liver oil for that matter), but not from the same cake made from flaxseed oil.

As you can see at 1:10 in my video, coconut oil may even be worse than tallow, or beef fat, but it is not as bad as butter. An interventional trial was published in March 2017: a month-long randomized, controlled, crossover study looking at the impact of two tablespoons per day of virgin coconut oil. The result? Coconut oil elevated cholesterol about 14 percent over the control, which was consistent with seven other interventional trials published to date in a 2016 review.

Hold on. Saturated fats can make HDL, the so-called good cholesterol, go up, so what’s the problem? The problem is that it doesn’t seem to help. Having a high blood HDL level is “no longer regarded as protective.” What? Wait a second. Higher HDL levels are clearly associated with lower risk of heart disease, as you can see at 2:01 in my video. In fact, HDL levels “are among the most consistent and robust predictors of CVD [cardiovascular disease] risk.” Ah, but there are two types of risk factors: causal and non-causal. Association does not mean causation—that is, just because two things are tightly linked, it doesn’t mean one causes the other.

Let me give you an example, which you can see at 2:30 in my video. I bet that the number of ashtrays someone owns is an excellent predictor of lung cancer risk and that study after study would show that link. But, that does not mean that if you intervene and lower the number of ashtrays someone has, their lung cancer risk will drop, because it’s not the ashtrays that are causing the cancer, but the smoking. The ashtrays are just a marker of smoking, an indicator of smoking, as opposed to playing a causal role in the disease. So, just like having a high number of running shoes and gym shorts might predict a lower risk of heart attack, having a high HDL also predicts a lower risk of heart attack. But, raising HDL, just like raising the number of gym shorts, wouldn’t necessarily affect disease risk. How do you differentiate between causal and non-causal risk factors? You put them to the test. The reason we know LDL cholesterol truly is bad is because people who were just born with genetically low LDL cholesterol end up having a low risk of heart disease. And, if you intervene and actively lower people’s LDL through diet or drugs, their heart disease risk drops—but not so with HDL.

People who live their whole lives with high HDL levels don’t appear to have a lower risk of heart attack, and if you give people a drug that increases their HDL, it doesn’t help. That’s why we used to give people high-dose niacin—to raise their HDL. But, it’s “time to face facts.” The “lack of benefit of raising the HDL cholesterol level with the use of niacin…seriously undermine[s] the hypothesis that HDL cholesterol is a causal risk factor.” In simple terms: “High HDL may not protect the heart.” We should concentrate on lowering LDL. So, specifically, as this relates to coconut oil, the increase in HDL “is of uncertain clinical relevance,” but the increase in LDL you get from eating coconut oil “would be expected to have an adverse effect” on atherosclerotic cardiovascular disease risk.

But, what about the MCTs, the medium-chain triglycerides? Proponents of coconut oil, who lament “that ‘coconut oil causes heart disease’ has created this bad image of [their] national exports,” assert that the medium-chain triglycerides, the shorter saturated fats found in coconut oil, aren’t as bad as the longer-chain saturated fats in meat and dairy. And, what about that study that purported to show low rates of heart disease among Pacific Islanders who ate large amounts of coconuts? I cover both of those topics in my video What About Coconuts, Coconut Milk, and Coconut Oil MCTs?.


I love topics that give me an excuse to talk about scientific concepts more generally, like various study designs in my video Prostate Cancer and Organic Milk vs. Almond Milk or my discussion of direct versus indirect risk factors in this one.

How do we know LDL is bad? Check out How Do We Know That Cholesterol Causes Heart Disease?.

But, wait. Isn’t the whole saturated fat thing bunk? No. See:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

What About Coconuts, Coconut Milk, and Coconut Oil MCTs?

Do the medium-chain triglycerides in coconut oil and the fiber in flaked coconut counteract the negative effects on cholesterol and artery function?

Studies of populations who eat a lot of coconuts are “frequently cited” by those who sell coconut oil “as evidence that coconut oil does not have negative effects on cardiovascular health.” For example, there was an apparent absence of stroke and heart disease on the island of Kativa in Papua New Guinea. What were they eating? Their diets centered around tubers, like sweet potatoes, with fruits, greens, nuts, corn, and beans. Although they ate fish a few times a week, they were eating a largely whole food plant-based diet. It’s no wonder they may have had such low rates of artery disease. And, one of the whole foods they were eating was coconut, not coconut oil.

Now, if you go to Pukapuka, even more coconuts are eaten. In fact, as you can see at 0:51 in my video What About Coconuts, Coconut Milk, and Coconut Oil MCTs?, there’s even an island where coconuts make up most of what people eat—and they do get high cholesterol. How can a population eating 87 percent plant-based, with no dairy and only rare consumption of red meat, chicken, and eggs, have cholesterol levels over 200? Well, they’re eating all those coconuts every day. What are their disease rates like? We don’t know. There are no clinical surveys, no epidemiological death data, and no autopsies. Some EKGs were taken, which can sometimes pick up evidence of past heart attacks, but they found few abnormalities. The sample was too small to be a definitive study, though. And, even if they did have low disease rates, they weren’t eating coconut oil—they were eating coconut in its whole form.

Coconut oil proponents pointing to these studies is like the high fructose corn syrup lobby pointing to studies of healthy populations who eat corn on the cob or the sugar industry pointing to studies on fruit consumption and saying you can eat all the refined sugar you want. But fruit has fiber and so do coconuts. Just as adding psyllium fiber (Metamucil) to coconut oil can help blunt the adverse effects on cholesterol, fiber derived from defatted coconut itself can reduce cholesterol levels as much as oat bran. What’s more, the plant protein in coconuts, which is also missing from the oil, may help explain why whole coconuts may not have the same effects on cholesterol. Although coconut fat in the form of powdered coconut milk may not have the same effects on cholesterol as coconut oil, frequent consumption, defined as three or more times a week, has been associated with increased risk of vascular disease, stroke, and heart disease. And, no wonder, as coconut milk may acutely impair artery function as badly as a sausage and egg McMuffin.

Researchers tested three different meals including a Western high-fat meal that “consisted of an Egg McMuffin®, Sausage McMuffin®, 2 hash brown patties and a non-caffeinated beverage (McDonald’s Corporation)” a local high-fat meal, and an “isocaloric low-fat meal.” The study was conducted in Singapore, so the more traditional local high-fat meal was rice cooked in coconut milk and served with anchovies and an egg. These two different high-fat meals were put up against the same amount of calories in an unhealthy low-fat meal of Frosted Flakes, skim milk, and juice. At 3:21 in my video, you can see the artery function—that is, its ability to relax normally—before and after eating each of the three meals. Researchers found that artery function is significantly crippled within hours of consuming the McMuffins and also the local high-fat meal with coconut milk. So, whether the fat is mostly from meat and oil or from coconut milk, the arteries clamped down similarly, whereas that horrible sugary breakfast had no bad effect on artery function. Why? Because as terrible as the Frosted Flakes meal was, it had no saturated fat at all. (It also didn’t have contain any eggs, so that might have helped, too.)

Coconut oil proponents also try to argue that coconut oil has MCTs, medium-chain triglycerides, which are shorter-chain saturated fats that aren’t as bad as the longer-chain saturated fats in meat and dairy. You can’t apply the MCT research to coconut oil, though. Why not? Well, MCT oil is composed of MCTs—about 50 percent of the medium-chain fat caprylic acid and the other 50 percent of the MCT capric acid—whereas those MCTs make up only about 10 percent of coconut oil. Most of coconut oil is the cholesterol-raising, longer-chain saturated fats, lauric and myristic. “It is therefore inaccurate to consider coconut oil to contain either predominantly medium-chain fatty acids or predominantly medium-chain triglycerides. Thus, the evidence on medium-chain triglycerides cannot be extrapolated to coconut oil.”

It’s actually quite “a common misconception” that the saturated fat in coconut oil is comprised of mainly MCTs. Actually, as we discussed, coconut oil is mainly lauric and myristic, both of which have potent bad LDL cholesterol-raising effects. “Coconut oil should therefore not be advised for people who should or want to reduce their risk of CHD,” coronary heart disease, which is the number-one killer of U.S. men and women. The beef industry, for example, loves to argue that beef fat contains stearic acid, a type of saturated fat that doesn’t raise cholesterol. Yes, but it also has palmitic and myristic acids that, like lauric acid, do raise cholesterol, as you can see at 5:12 in my video.

If you compare the effects of different saturated fats, as you can see at 5:29 in my video, stearic acid does have a neutral effect on LDL, but palmitic, myristic, and lauric acids shoot it up—and, frankly, so may MCT oil itself, as it bumps up LDL 15 percent compared to control. Bottom line? “Popular belief”—spread by the coconut oil industry—“holds that coconut oil is healthy, a notion not supported by scientific data.” The science just doesn’t support it.

So, basically, “coconut oil should be viewed no differently” from animal sources of dietary saturated fat. A recent review published in the Journal of the American College of Cardiology put it even more simply in its recommendations for patients. When it comes to coconut oil, “avoid.”

Okay, but doesn’t saturated fat boost HDL, the so-called good cholesterol? Check out Coconut Oil and the Boost in HDL “Good” Cholesterol.


Isn’t coconut oil supposed to be good for Alzheimer’s, though? See my video Does Coconut Oil Cure Alzheimer’s?

If you want to learn more about the original McMuffin artery studies, see The Leaky Gut Theory of Why Animal Products Cause Inflammation.

You may also be interested in Flashback Friday: Coconut Oil and Abdominal Fat.

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

Do the Pros of Brown Rice Outweigh the Cons of Arsenic?

Are there unique benefits to brown rice that would justify keeping it in our diet despite the arsenic content?

For years, warnings had been given about the arsenic levels in U.S. rice potentially increasing cancer risk, but it had never been put to the test until a study out of Harvard. The finding? “Long-term consumption of total rice, white rice or brown rice[,] was not associated with risk of developing cancer in US men and women.” This was heralded as good news. Indeed, no increased cancer risk found even among those eating five or more servings of rice per week. But, wait a second: Brown rice is a whole grain, a whole plant food. Shouldn’t brown rice be protective and not just neutral? I discuss this in my video Do the Pros of Brown Rice Outweigh the Cons of Arsenic?.

If you look at whole grains in general, there is “a significant inverse”—or protective—“association between total whole-grain intake and risk of mortality from total cancers,” that is, dying from cancer. My Daily Dozen recommendation of at least three servings of whole grains a day was associated with a 10 percent lower risk of dying from cancer, a 25 percent lower risk of dying from heart attacks or strokes, and a 17 percent lower risk of dying prematurely across the board, whereas rice consumption in general was not associated with mortality and was not found to be protective against heart disease or stroke. So, maybe this lack of protection means that the arsenic in rice is increasing disease risk, so much so that it’s cancelling out some of the benefits of whole-grain brown rice.

Consumer Reports suggested moderating one’s intake of even brown rice, but, given the arsenic problem, is there any reason we should go out of our way to retain any rice in our diet at all? With all of the other whole grain options out there, should we just skip the rice completely? Or, are there some unique benefits we can get from rice that would justify continuing to eat it, even though it has ten times more arsenic than other grains?

One study showed that “a brown rice based vegan diet” beat out the conventional Diabetes Association diet, even after adjusting for the extra belly fat lost by the subjects on the vegan diet, but that may have been due to the plant-based nature of their diet rather than just how brown rice-based it was.

Another study found a profound improvement in insulin levels after just five days eating brown rice compared to white rice, but was that just because the white rice made people worse? No, the brown rice improved things on its own, but the study was done with a South Indian population eating a lot of white rice to begin with, so this may have indeed been at least in part a substitution effect. And yet another study showed that instructing people to eat about a cup of brown rice a day “could significantly reduce weight, waist and hip circumference, BMI, Diastole blood pressure,” and inflammation—and not just because it was compared to white. However, a larger, longer study failed to see much more than a blood pressure benefit, which was almost as impressive in the white-rice group, so, overall, not too much to write home about.

Then, another study rolled around—probably the single most important study on the pro-rice sideshowing a significant improvement in artery function after eight weeks of eating about a daily cup of brown rice, but not white, as you can see at 3:18 in my video, and sometimes even acutely. If you give someone a meal with saturated fat and white rice, you can get a drop in artery function within an hour of consumption if you have some obesity-related metabolic derangements. But, if you give brown rice instead of white, artery function appears protected against the adverse effects of the meal. Okay, so brown rice does show benefits in interventional studies, but the question is whether it shows unique benefits. Instead, what about oatmeal or whole wheat?

Well, first, researchers needed to design an artery-crippling meal, high in saturated fat. They went with a Haagen Daaz, coconut cream, and egg milkshake given with a bowl of oatmeal or “a comparable bowl of whole rolled wheat.” What do you think happened? Do you think these whole grains blocked the artery-damaging effects like the brown rice did? The whole oats worked, but the whole wheat did not. So, one could argue that brown rice may have an edge over whole wheat. Do oats also have that beneficial long-term effect that brown rice did? The benefit was of a similar magnitude but did not reach statistical significance.

So, what’s the bottom line? Until we know more, my current thinking on the matter is that if you really like rice, you can moderate your risk by cutting down, choosing lower arsenic varieties, and cooking it in a way to lower exposure even further. But, if you like other whole grains just as much and don’t really care if you have rice versus quinoa or another grain, I’d choose the lower arsenic option.

Tada! Done with arsenic in the food supply—for now. Should the situation change, I’ll produce another video on the latest news. Make sure you’re subscribed so you don’t miss any updates.


Here are all 13 videos in the series, in case you missed any or want to go back and review:

And you may be interested in Benefits of Turmeric for Arsenic Exposure.

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations: